Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1107636 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28891376.fastq.gz | Fastqsanger.gz | |||
| SRR28891376_1.fastq.gz | Fastqsanger.gz | |||
| SRR28891376_2.fastq.gz | Fastqsanger.gz | |||
| SRR28891377_1.fastq.gz | Fastqsanger.gz | |||
| SRR28891377_2.fastq.gz | Fastqsanger.gz |
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Project description:Opportunistic pathogens resistant to antibiotics
| PRJNA865540 | ENA
Project description:To examine the role of hepatpcyte growth factor activator inhibitor type 1 (HAI-1) in cancer, we analyzed effect of HAI-1 silencing on gene expression profiles of human oral squamous cell carcinoma cell line, SAS. We used short hairpin RNA (shRNA) directed against HAI-1 mRNA. We constructed retroviral vectors which showed stable and significant silencing effects on HAI-1 genes of SAS. Microarray data of the expression profiles of duplicated experiments of HAI-1-knockdown SAS with that from the control cell are shown.
2012-01-25 | GSE32142 | GEO
Project description:A large-scale parallel expression analysis was conducted to elucidate Mla-specified responses to powdery mildew infection using 22K Barley1 GeneChip probe arrays. Our goal was to identify genes differentially expressed in incompatible (resistant) vs. compatible (susceptible) and Mla-specified Rar1-dependent vs. -independent interactions. A split-split-plot design with 108 experimental units (3 replications x 2 isolates x 3 genotypes x 6 time points) was used to profile near-isogenic lines containing the Mla1, Mla6, and Mla13 resistance specificities in response to inoculation with the Blumeria graminis f. sp. hordei (Bgh) isolates 5874 (AvrMla1, AvrMla6) and K1 (AvrMla1, AvrMla13). ****[PLEXdb(http://www.plexdb.org) has submitted this series at GEO on behalf of the original contributor, Rico Caldo. The equivalent experiment is BB4 at PLEXdb.] genotype: CI 16137 (Mla1) - pathogen isolates: Bgh 5874 - time: 0 hai(3-replications); genotype: CI 16137 (Mla1) - pathogen isolates: Bgh 5874 - time: 8 hai(3-replications); genotype: CI 16137 (Mla1) - pathogen isolates: Bgh 5874 - time: 16 hai(3-replications); genotype: CI 16137 (Mla1) - pathogen isolates: Bgh 5874 - time: 20 hai(3-replications); genotype: CI 16137 (Mla1) - pathogen isolates: Bgh 5874 - time: 24 hai(3-replications); genotype: CI 16137 (Mla1) - pathogen isolates: Bgh 5874 - time: 32 hai(3-replications); genotype: CI 16137 (Mla1) - pathogen isolates: Bgh K1 - time: 0 hai(3-replications); genotype: CI 16137 (Mla1) - pathogen isolates: Bgh K1 - time: 8 hai(3-replications); genotype: CI 16137 (Mla1) - pathogen isolates: Bgh K1 - time: 16 hai(3-replications); genotype: CI 16137 (Mla1) - pathogen isolates: Bgh K1 - time: 20 hai(3-replications); genotype: CI 16137 (Mla1) - pathogen isolates: Bgh K1 - time: 24 hai(3-replications); genotype: CI 16137 (Mla1) - pathogen isolates: Bgh K1 - time: 32 hai(3-replications); genotype: CI 16151 (Mla6) - pathogen isolates: Bgh 5874 - time: 0 hai(3-replications); genotype: CI 16151 (Mla6) - pathogen isolates: Bgh 5874 - time: 8 hai(3-replications); genotype: CI 16151 (Mla6) - pathogen isolates: Bgh 5874 - time: 16 hai(3-replications); genotype: CI 16151 (Mla6) - pathogen isolates: Bgh 5874 - time: 20 hai(3-replications); genotype: CI 16151 (Mla6) - pathogen isolates: Bgh 5874 - time: 24 hai(3-replications); genotype: CI 16151 (Mla6) - pathogen isolates: Bgh 5874 - time: 32 hai(3-replications); genotype: CI 16151 (Mla6) - pathogen isolates: Bgh K1 - time: 0 hai(3-replications); genotype: CI 16151 (Mla6) - pathogen isolates: Bgh K1 - time: 8 hai(3-replications); genotype: CI 16151 (Mla6) - pathogen isolates: Bgh K1 - time: 16 hai(3-replications); genotype: CI 16151 (Mla6) - pathogen isolates: Bgh K1 - time: 20 hai(3-replications); genotype: CI 16151 (Mla6) - pathogen isolates: Bgh K1 - time: 24 hai(3-replications); genotype: CI 16151 (Mla6) - pathogen isolates: Bgh K1 - time: 32 hai(3-replications); genotype: CI 16155 (Mla13) - pathogen isolates: Bgh 5874 - time: 0 hai(3-replications); genotype: CI 16155 (Mla13) - pathogen isolates: Bgh 5874 - time: 8 hai(3-replications); genotype: CI 16155 (Mla13) - pathogen isolates: Bgh 5874 - time: 16 hai(3-replications); genotype: CI 16155 (Mla13) - pathogen isolates: Bgh 5874 - time: 20 hai(3-replications); genotype: CI 16155 (Mla13) - pathogen isolates: Bgh 5874 - time: 24 hai(3-replications); genotype: CI 16155 (Mla13) - pathogen isolates: Bgh 5874 - time: 32 hai(3-replications); genotype: CI 16155 (Mla13) - pathogen isolates: Bgh K1 - time: 0 hai(3-replications); genotype: CI 16155 (Mla13) - pathogen isolates: Bgh K1 - time: 8 hai(3-replications); genotype: CI 16155 (Mla13) - pathogen isolates: Bgh K1 - time: 16 hai(3-replications); genotype: CI 16155 (Mla13) - pathogen isolates: Bgh K1 - time: 20 hai(3-replications); genotype: CI 16155 (Mla13) - pathogen isolates: Bgh K1 - time: 24 hai(3-replications); genotype: CI 16155 (Mla13) - pathogen isolates: Bgh K1 - time: 32 hai(3-replications)
2011-11-22 | E-GEOD-33396 | biostudies-arrayexpress
Project description:Experimental design: 1 genotype: PI- (resistant USDA Plant Introduction (PI462312) line containing SBR Rpp3 resistance gene) 3 treatments: Virulent soybean rust (Phakopsora pachyrhizi Tw80-2) challenge, avirulent soybean rust challenge (Hw94-1) & mock infection 3 replications 6 time points: 12, 24, 72, 144, 216 and 288 hours after inoculation TOTAL: 54 Affymetrix GeneChip(R) Soybean Genome Arrays Mock treatment: 0.01% Tween 20 Hawaii 94 treatment: 500,000 spores per ml in 0.01% Tween 20 Taiwan 80-2 treatment: 500,000 spores per ml in 0.01% Tween 20 ****[PLEXdb(http://www.plexdb.org) has submitted this series at GEO on behalf of the original contributor, Martijn van de Mortel (for Steve Whitham). The equivalent experiment is GM36 at PLEXdb.] pathogen isolates: Mock - time: 12 hai(3-replications); pathogen isolates: Mock - time: 24 hai(3-replications); pathogen isolates: Mock - time: 72 hai(3-replications); pathogen isolates: Mock - time: 144 hai(3-replications); pathogen isolates: Mock - time: 216 hai(3-replications); pathogen isolates: Mock - time: 288 hai(3-replications); pathogen isolates: Taiwan 80-2 (vir) - time: 12 hai(3-replications); pathogen isolates: Taiwan 80-2 (vir) - time: 24 hai(3-replications); pathogen isolates: Taiwan 80-2 (vir) - time: 72 hai(3-replications); pathogen isolates: Taiwan 80-2 (vir) - time: 144 hai(3-replications); pathogen isolates: Taiwan 80-2 (vir) - time: 216 hai(3-replications); pathogen isolates: Taiwan 80-2 (vir) - time: 288 hai(3-replications); pathogen isolates: Hawaii 94-1 (avir) - time: 12 hai(3-replications); pathogen isolates: Hawaii 94-1 (avir) - time: 24 hai(3-replications); pathogen isolates: Hawaii 94-1 (avir) - time: 72 hai(3-replications); pathogen isolates: Hawaii 94-1 (avir) - time: 144 hai(3-replications); pathogen isolates: Hawaii 94-1 (avir) - time: 216 hai(3-replications); pathogen isolates: Hawaii 94-1 (avir) - time: 288 hai(3-replications)
2011-11-28 | E-GEOD-29740 | biostudies-arrayexpress
Project description:TITLE: Transcriptional profiling of Rgene-mediated responses in rice PROJECT DESCRIPTION: The dominant gene Xa7 and the recessive gene xa5 of rice confer resistance to several races of the bacterial blight pathogen Xanthomonas oryzae pv. oryzae (Xoo). To reveal the modes of action and the defense responses these genes initiate, we decided to obtain the global transcriptional profiles of the rice cultivars IRBB7, IRBB5 (which harbor Xa7 and xa5, respectively) and IR24 undergoing early infection by the Xoo Race 2 strain PXO86. Both IRBB7 and IRBB5 are resistant to PXO86 (which carry the corresponding avirulence genes avrXa7 and avrxa5), whereas IR24 is susceptible. We inoculated by vacuum infiltration the three rice cultivars ten days after seed germination (or 2 weeks after sowing) and collected inoculated tissue at 5 different timepoints within the first day after inoculation. The transcriptional profiles obtained will provide valuable insight into the similarities and differences between incompatible interactions mediated by a dominant and a recessive Rgene, in comparison to a compatible interaction. ****[PLEXdb(http://www.plexdb.org) has submitted this series at GEO on behalf of the original contributor, David O Nino-Liu. The equivalent experiment is OS4 at PLEXdb.] genotype: IR24 - time: 0 hai(3-replications); genotype: IR24 - time: 3 hai(3-replications); genotype: IR24 - time: 6 hai(3-replications); genotype: IR24 - time: 12 hai(3-replications); genotype: IR24 - time: 24 hai(3-replications); genotype: IRBB5 - time: 0 hai(3-replications); genotype: IRBB5 - time: 3 hai(3-replications); genotype: IRBB5 - time: 6 hai(3-replications); genotype: IRBB5 - time: 12 hai(3-replications); genotype: IRBB5 - time: 24 hai(3-replications); genotype: IRBB7 - time: 0 hai(3-replications); genotype: IRBB7 - time: 3 hai(3-replications); genotype: IRBB7 - time: 6 hai(3-replications); genotype: IRBB7 - time: 12 hai(3-replications); genotype: IRBB7 - time: 24 hai(3-replications)
2011-11-22 | E-GEOD-33411 | biostudies-arrayexpress
Project description:Barley florets (cv. Morex) were treated with 2.0 microgram deoxynivalenol per floret via a 10 microliter solution or mock inoculated with water. Samples were collected at 1, 12, 24, and 48 hours after inoculation. ****[PLEXdb(http://www.plexdb.org) has submitted this series at GEO on behalf of the original contributor, Stephanie A. Gardiner. The equivalent experiment is BB62 at PLEXdb.] time: 1 hai - treated or untreated: Deoxynivalenol(3-replications); time: 1 hai - treated or untreated: Water(3-replications); time: 12 hai - treated or untreated: Deoxynivalenol(3-replications); time: 12 hai - treated or untreated: Water(3-replications); time: 24 hai - treated or untreated: Deoxynivalenol(3-replications); time: 24 hai - treated or untreated: Water(3-replications); time: 48 hai - treated or untreated: Deoxynivalenol(3-replications); time: 48 hai - treated or untreated: Water(3-replications)
2011-11-22 | E-GEOD-33405 | biostudies-arrayexpress
Project description:Here, we reveal that the Caenorhabditis elegans ADAR proteins promote survival of animals exposed to several opportunistic human pathogens. Our data indicate that ADARs help maintain proper levels of cuticular collagen genes, which in turn affects defense of the nematode to these bacteria.
2023-04-01 | GSE223919 | GEO
Project description:RESEARCH SUMMARY Bacterial blight and bacterial leaf streak, two of the most serious diseases of rice, are caused by Xanthomonas oryzae pathovar (pv.) oryzae (Xoo) and X. oryzae pv. oryzicola (Xoc) respectively. Xoo is a vascular pathogen that invades the xylem, whereas Xoc is non-vascular and colonizes the mesophyll apoplast. These distinctive types of infection represent the two most common ways plant pathogenic bacteria produce disease. As closely related pathogens of a model plant host, Xoo and Xoc constitute a powerful comparative system. We hypothesize that tissue-specific susceptibility to pathogenic bacteria can be explained partially by differential host responses during infection. To establish the global structure of susceptible responses to infection by Xoo and Xoc, we used the Affymetrix Rice Genome Array to analyze the abundance of transcripts in rice plants over four days after inoculation with virulent strains. MATERIAL AND METHODS - Plant Material: Oryza sativa ssp. japonica cv. Nipponbare plants were grown in pots containing LC-1 soil mixture, and arranged in flats of 20 pots, in growth chambers under a 12-h, 28ºC light and a 12-h, 25ºC dark cycle. To allow inversion of the flats for inoculation (modified dip-inoculation method, Niño-Liu et al, 2005, Journal of Phytopathology) seeds were sown through 1-cm perforations in a fibreglass tray resting on top of the pots. Peters Professional Fertilizer and iron chelate micronutrient were applied with watering every two days at rates of 0.25 and 4.5 g/L, respectively, until the day before inoculation. - Bacterial Strains and preparation of inoculum: Xoo strain PXO99A and Xoc strain BLS256 were used. For each, a single colony from a glucose yeast extract (GYE) agar plate was transferred to 5 ml of GYE liquid medium and incubated for 24 h at 28ºC with constant shaking at 250 rpm. Subsequently, 2 ml of this culture was transferred to 300 ml of fresh GYE liquid medium and incubated as above for an additional 18 h. Cells were pelleted by centrifugation at 4000 rpm. for 10 min, washed twice and resuspended in sterile 10 mm MgCl2 to an OD600 of 0.05, yielding 7 liters of inoculum. Tween-20 was added to a final concentration of 0.5%. - Modified dip-inoculation method: Fourteen days after sowing, and 2 h after the beginning of the light period, seedlings were inverted into inoculum, one flat each for Xoo, Xoc and Mock inoculum consisting of sterile 10 mM MgCl2 with 0.5% Tween-20, and vaccuum infiltrated at 500mm Hg for two minutes, two consecutive times, in a custom-made chamber. Following inoculation, plants were returned to the growth chamber. During growth, plants were cycled weekly in the same order through three growth chambers. In this way all plants could be incubated in the same final chamber following inoculation. For each replicate, position of the flats in the growth chamber (from left to right, used also for the order of inoculation and harvest) was determined by a split-plot design. - Timepoints, tissue collection: Within flats, assignment of pots for the harvest of inoculated tissue at 2, 4, 8, 24 and 96 h was made using a separate randomized complete block design. Tissue was harvested from plants in four pots (approximately 2g fresh weight) for each timepoint per inoculum per replication. Harvested tissue was immediately frozen in liquid nitrogen and stored at -80ºC until processing. - RNA isolation, purification, labeling, hybridizations, scanning: Total RNA was initially isolated from frozen whole plant tissue using the hot TRIzol reagent protocol for barley as described by Caldo et al (Plant Cell, 2004). The RNA was purified using Qiagen RNeasy spin columns, and adjusted to a final concentration of 1 ug/uL. Probe synthesis, labeling, and hybridization were performed at the Iowa State University GeneChip Core facility. ACKNOWLEDGEMENTS This work was supported by a grant (0227357) from the Plant Genome Research Program of the National Science Foundation. ****[PLEXdb(http://www.plexdb.org) has submitted this series at GEO on behalf of the original contributor, David O Niño-Liu. The equivalent experiment is OS3 at PLEXdb.] XOC - time: 2 hai (4-replications) XOC - time: 4 hai (4-replications) XOC - time: 8 hai (4-replications) XOC - time: 24 hai (4-replications) XOC - time: 96 hai (4-replications) XOO - time: 2 hai (4-replications) XOO - time: 4 hai (4-replications) XOO - time: 8 hai (4-replications) XOO - time: 24 hai (4-replications) XOO - time: 96 hai (4-replications) MOCK - time: 2 hai (4-replications) MOCK - time: 4 hai (4-replications) MOCK - time: 8 hai (4-replications) MOCK - time: 24 hai (4-replications) MOCK - time: 96 hai (4-replications)
2009-06-24 | E-GEOD-16793 | biostudies-arrayexpress
Project description:The mammalian immune system is constantly challenged by signals from both pathogenic and non-pathogenic microbes. Many of these non-pathogenic microbes have pathogenic potential if the immune system is compromised. The importance of type I interferons (IFNs) in orchestrating innate immune responses to pathogenic microbes has become clear in recent years. However, the control of opportunistic pathogens – and especially intracellular bacteria – by type I IFNs remains less appreciated. In this study, we use the opportunistic, Gram-negative bacterial pathogen Burkholderia cenocepacia (Bc) to show that type I IFNs are capable of limiting bacterial replication in macrophages, preventing illness in immunocompetent mice. Sustained type I IFN signaling through cytosolic receptors allows for increased expression of autophagy and linear ubiquitination mediators, which slows bacterial replication. Transcriptomic analyses and in vivo studies also show that LPS stimulation does not replicate the conditions of intracellular Gram-negative bacterial infection as it pertains to type I IFN stimulation or signaling. This study highlights the importance of type I IFNs in protection against opportunistic pathogens through innate immunity, without the need for damaging inflammatory responses.
2021-01-19 | GSE165020 | GEO